NSG 530 Exam 4 Actual Exam V1 | NSG 530 Advanced
Pathophysiology (NSG530 Exam 4) [PDF] | Wilkes University
1. A 68-year-old male presents with sudden onset of right-sided weakness and aphasia. A CT
scan is negative for hemorrhage, and the diagnosis of ischemic stroke is made. Which of the
following describes the ‘penumbra’ in this pathophysiological context?
A. The zone of hypoperfused tissue surrounding the core that may be salvaged with
reperfusion.
B. The central core of necrotic tissue that is irreversibly damaged.
C. The area of the brain where collateral circulation has completely failed.
D. A region of hyperemic tissue caused by inflammatory cytokines.
Answer: A
Rationale: The ischemic penumbra represents the tissue surrounding the necrotic core
that receives enough blood flow to remain viable but not enough to function properly. If
reperfusion is not achieved quickly, the metabolic demands of these cells will eventually
lead to cell death and expansion of the infarct. Salvaging this area is the primary goal of
acute stroke interventions like thrombolysis or mechanical thrombectomy.
2. Following a traumatic brain injury, a patient develops increased intracranial pressure (ICP).
According to the Monro-Kellie hypothesis, what occurs first to compensate for an expanding
intracranial mass?
A. Expansion of the cranial vault to accommodate the volume.
B. Increased production of CSF to buffer the pressure.
C. Displacement of cerebrospinal fluid (CSF) into the spinal subarachnoid space.
D. Reduction in arterial blood flow to decrease cerebral volume.
Answer: C
Rationale: The Monro-Kellie hypothesis states that the sum of volumes of brain, CSF, and
intracerebral blood is constant. Initial compensation for an increased volume involves the
displacement of CSF into the spinal canal and the shunting of venous blood out of the skull.
Once these compensatory mechanisms are exhausted, ICP rises rapidly, leading to
decreased cerebral perfusion pressure.
3. A 24-year-old patient is diagnosed with generalized tonic-clonic seizures. What is the
primary neurochemical mechanism underlying the initiation of a seizure?
A. Hypersynchronization of neurons due to an imbalance between excitatory and inhibitory
neurotransmission.
,B. Excessive inhibition by Gamma-aminobutyric acid (GABA).
C. Localized destruction of the myelin sheath in the motor cortex.
D. Excessive accumulation of dopamine in the basal ganglia.
Answer: A
Rationale: Seizures are characterized by a sudden, excessive, and hypersynchronous
discharge of cerebral neurons. This is typically caused by an imbalance where excitatory
neurotransmission (often via glutamate) outweighs inhibitory neurotransmission (often
via GABA). The paroxysmal depolarization shift allows for the spread of electrical activity
across neuronal networks.
4. A patient with Alzheimer’s disease shows significant cognitive decline. Pathologically, this
condition is associated with which of the following?
A. Extracellular amyloid-beta plaques and intracellular neurofibrillary tangles.
B. Dopaminergic depletion in the substantia nigra.
C. Demyelination of the peripheral nerves by T-cells.
D. Degeneration of upper and lower motor neurons.
Answer: A
Rationale: Alzheimer’s disease is characterized by the accumulation of neuritic plaques
containing amyloid-beta protein in the extracellular space. Additionally, tau protein
becomes hyperphosphorylated, forming neurofibrillary tangles within the neurons
themselves. These changes lead to synaptic loss and significant cortical atrophy,
particularly in the hippocampus and temporal lobes.
5. Which clinical manifestation is part of Cushing’s Triad, signaling an impending brain
herniation due to severely increased ICP?
A. Tachycardia, hypertension, and tachypnea.
B. Bradycardia, widened pulse pressure, and irregular respirations.
C. Hypotension, bradycardia, and Cheyne-Stokes breathing.
D. Tachycardia, hypotension, and fixed dilated pupils.
Answer: B
Rationale: Cushing’s Triad is a late sign of increased intracranial pressure and brainstem
compression. It consists of hypertension with a widened pulse pressure, bradycardia, and
abnormal respiratory patterns. This reflex occurs as the body attempts to maintain
cerebral perfusion by increasing systemic blood pressure while the baroreceptors respond
to that increase by slowing the heart rate.
, 6. A patient presents with resting tremor, bradykinesia, and ‘cogwheel’ rigidity. Which
neurotransmitter deficiency is the hallmark of this disorder?
A. Acetylcholine
B. Norepinephrine
C. Serotonin
D. Dopamine
Answer: D
Rationale: Parkinson’s disease involves the progressive loss of dopaminergic neurons in
the substantia nigra pars compacta of the basal ganglia. This loss disrupts the balance
between the direct and indirect pathways of motor control. The result is the classic triad of
tremor, rigidity, and bradykinesia, which are often treated with dopamine precursors like
levodopa.
7. A 32-year-old female presents with fatigue and paresthesia. An MRI reveals multiple areas
of demyelination in the central nervous system. Which cell type is targeted by the immune
system in this condition?
A. Oligodendrocytes
B. Schwann cells
C. Astrocytes
D. Microglia
Answer: A
Rationale: Multiple Sclerosis (MS) is an autoimmune disorder where T-cells and B-cells
attack the myelin sheath in the central nervous system. Oligodendrocytes are the cells
responsible for producing myelin in the CNS, and their destruction leads to slowed nerve
conduction and plaque formation. This contrasts with Guillain-Barré syndrome, where
Schwann cells in the peripheral nervous system are targeted.
8. In the pathophysiology of Myasthenia Gravis, muscle weakness occurs because:
A. Motor neurons in the spinal cord undergo apoptosis.
B. Calcium channels are blocked, preventing the release of acetylcholine.
C. Autoantibodies block or destroy acetylcholine receptors at the neuromuscular junction.
D. Muscle fibers lose the ability to store glycogen.
Answer: C
Rationale: Myasthenia Gravis is a Type II hypersensitivity disorder where IgG
autoantibodies are produced against the postsynaptic acetylcholine receptors (AChR). This
Pathophysiology (NSG530 Exam 4) [PDF] | Wilkes University
1. A 68-year-old male presents with sudden onset of right-sided weakness and aphasia. A CT
scan is negative for hemorrhage, and the diagnosis of ischemic stroke is made. Which of the
following describes the ‘penumbra’ in this pathophysiological context?
A. The zone of hypoperfused tissue surrounding the core that may be salvaged with
reperfusion.
B. The central core of necrotic tissue that is irreversibly damaged.
C. The area of the brain where collateral circulation has completely failed.
D. A region of hyperemic tissue caused by inflammatory cytokines.
Answer: A
Rationale: The ischemic penumbra represents the tissue surrounding the necrotic core
that receives enough blood flow to remain viable but not enough to function properly. If
reperfusion is not achieved quickly, the metabolic demands of these cells will eventually
lead to cell death and expansion of the infarct. Salvaging this area is the primary goal of
acute stroke interventions like thrombolysis or mechanical thrombectomy.
2. Following a traumatic brain injury, a patient develops increased intracranial pressure (ICP).
According to the Monro-Kellie hypothesis, what occurs first to compensate for an expanding
intracranial mass?
A. Expansion of the cranial vault to accommodate the volume.
B. Increased production of CSF to buffer the pressure.
C. Displacement of cerebrospinal fluid (CSF) into the spinal subarachnoid space.
D. Reduction in arterial blood flow to decrease cerebral volume.
Answer: C
Rationale: The Monro-Kellie hypothesis states that the sum of volumes of brain, CSF, and
intracerebral blood is constant. Initial compensation for an increased volume involves the
displacement of CSF into the spinal canal and the shunting of venous blood out of the skull.
Once these compensatory mechanisms are exhausted, ICP rises rapidly, leading to
decreased cerebral perfusion pressure.
3. A 24-year-old patient is diagnosed with generalized tonic-clonic seizures. What is the
primary neurochemical mechanism underlying the initiation of a seizure?
A. Hypersynchronization of neurons due to an imbalance between excitatory and inhibitory
neurotransmission.
,B. Excessive inhibition by Gamma-aminobutyric acid (GABA).
C. Localized destruction of the myelin sheath in the motor cortex.
D. Excessive accumulation of dopamine in the basal ganglia.
Answer: A
Rationale: Seizures are characterized by a sudden, excessive, and hypersynchronous
discharge of cerebral neurons. This is typically caused by an imbalance where excitatory
neurotransmission (often via glutamate) outweighs inhibitory neurotransmission (often
via GABA). The paroxysmal depolarization shift allows for the spread of electrical activity
across neuronal networks.
4. A patient with Alzheimer’s disease shows significant cognitive decline. Pathologically, this
condition is associated with which of the following?
A. Extracellular amyloid-beta plaques and intracellular neurofibrillary tangles.
B. Dopaminergic depletion in the substantia nigra.
C. Demyelination of the peripheral nerves by T-cells.
D. Degeneration of upper and lower motor neurons.
Answer: A
Rationale: Alzheimer’s disease is characterized by the accumulation of neuritic plaques
containing amyloid-beta protein in the extracellular space. Additionally, tau protein
becomes hyperphosphorylated, forming neurofibrillary tangles within the neurons
themselves. These changes lead to synaptic loss and significant cortical atrophy,
particularly in the hippocampus and temporal lobes.
5. Which clinical manifestation is part of Cushing’s Triad, signaling an impending brain
herniation due to severely increased ICP?
A. Tachycardia, hypertension, and tachypnea.
B. Bradycardia, widened pulse pressure, and irregular respirations.
C. Hypotension, bradycardia, and Cheyne-Stokes breathing.
D. Tachycardia, hypotension, and fixed dilated pupils.
Answer: B
Rationale: Cushing’s Triad is a late sign of increased intracranial pressure and brainstem
compression. It consists of hypertension with a widened pulse pressure, bradycardia, and
abnormal respiratory patterns. This reflex occurs as the body attempts to maintain
cerebral perfusion by increasing systemic blood pressure while the baroreceptors respond
to that increase by slowing the heart rate.
, 6. A patient presents with resting tremor, bradykinesia, and ‘cogwheel’ rigidity. Which
neurotransmitter deficiency is the hallmark of this disorder?
A. Acetylcholine
B. Norepinephrine
C. Serotonin
D. Dopamine
Answer: D
Rationale: Parkinson’s disease involves the progressive loss of dopaminergic neurons in
the substantia nigra pars compacta of the basal ganglia. This loss disrupts the balance
between the direct and indirect pathways of motor control. The result is the classic triad of
tremor, rigidity, and bradykinesia, which are often treated with dopamine precursors like
levodopa.
7. A 32-year-old female presents with fatigue and paresthesia. An MRI reveals multiple areas
of demyelination in the central nervous system. Which cell type is targeted by the immune
system in this condition?
A. Oligodendrocytes
B. Schwann cells
C. Astrocytes
D. Microglia
Answer: A
Rationale: Multiple Sclerosis (MS) is an autoimmune disorder where T-cells and B-cells
attack the myelin sheath in the central nervous system. Oligodendrocytes are the cells
responsible for producing myelin in the CNS, and their destruction leads to slowed nerve
conduction and plaque formation. This contrasts with Guillain-Barré syndrome, where
Schwann cells in the peripheral nervous system are targeted.
8. In the pathophysiology of Myasthenia Gravis, muscle weakness occurs because:
A. Motor neurons in the spinal cord undergo apoptosis.
B. Calcium channels are blocked, preventing the release of acetylcholine.
C. Autoantibodies block or destroy acetylcholine receptors at the neuromuscular junction.
D. Muscle fibers lose the ability to store glycogen.
Answer: C
Rationale: Myasthenia Gravis is a Type II hypersensitivity disorder where IgG
autoantibodies are produced against the postsynaptic acetylcholine receptors (AChR). This
